The diabetic retinopathy is the main cause of blindness in the occidental world even if most diabetics do not become blind.
The first signs of the retinic change consist in the increase of the capillary permeability shown by the loss of the colouring matter within the vitreous humour after a fluorescein injection. Subsequently the occlusion of the retinic capillaries occurs with consequent formation of aneurysms sack- and spindle-shaped; moreover arteriovenous deviations can also occur.
The vascular lesions are accompanied by the proliferation of sprouts of endothelium cells and by the loss of the pericytes that surround and support the blood vessels.
Punctiform haemorrhages occur in the inner retinic areas, while the bleeding at the level of the more superficial layer of the nervous fibres causes lesions in the shape of flame, stain or line, while the pre-retinic haemorrhages show a typical look in the shape of a boot.
The diabetic retinopathy causes also two kinds of exudates: cottony exudates and hard exudates.
The first ones are individuated by the angiography as microinfarcts, i.e. as areas not sprinkled surrounded by a ring of broken capillaries. A sudden increase of the number of the cottony exudates represents a signal of unfavourable prognosis and can be the warning of a quick progression of the retinopathy.
The hard exudates are more common than the cottony exudates and indicate the leakage of serum proteins and of lipids from the damaged capillaries.
The vitreous haemorrhage and the detachment of the retina are the most severe complications of the diabetic retinopathy: a sudden loss of the visus in an eye is almost always caused by one of these lesions.
The frequency of the diabetic retinopathy depends on the duration of the diabetic disease; about 85% of the diabetic people suffers from retinopathy even if ophthalmologically distinguishable lesions do not sometimes appear also after 30 years of diabetes.
One of the mechanisms discovered by Hansen C. et al. on Horm. Metab. Res., 27, (12), 555-8, (1995) as a cause of the development of the diabetic microangiopathy lies in the lowering of the amount of glycosaminoglycans, heparan sulfates and dermatan sulfates, within the basal membrane of the capillary endothelium with consequent increase of the vasal permeability.
This mechanism has been described also in the retinic microvessels, mainly in the arterioles, and is considered one of the first steps in the development of the retinopathy. Tamsma J. T. et al. on Diabetologia, 37 (3), 313-20, (1994) showed how the decrease of the glycosaminoglycans, mainly of the heparan sulfate, is responsible for the change of the anionic charge in the glomerular basal membrane with consequent proteinuria and Cruickshanks K. J. et al. on Ophthalmology, 100, 862-7, (1993) have shown the relation between microalbuminuria and diabetic retinopathy that explains both the breakage of the haemato-retinic barrier and the plasmatic exudation in the retina.
U.S. Pat. No. 5,496,807 showed how the administration of sulodexide, a glycosaminoglycan made by a heparin like fraction and by dermatan sulfate, has significantly reduced the excretion of albumin in diabetic patients not dependent from insulin.
The effect of the administration of the sulodexide to patients suffering from diabetic retinopathy has now been investigated on the ground of the described observations.